Plaque can develop in a patient's cardiovascular system The plaque can be quite extensive and occlude a substantial length of the vessel. Additionally, the plaque may be inflamed and unstable, such plaque being subject to rupture, erosion or ulceration which can cause the patient to experience a myocardial infarction, thrombosis or other traumatic and unwanted effects. Such inflamed and unstable plaques are commonly known as vulnerable atherosclerotic plaques. Furthermore, relative blood viscosity rises and aggregation of platelets increases with temperature increases (Dintefass L. Rheology of Blood in Diagnostic and Preventive Medicine London, UK: Butterworths; 1976;66-74).
Previous ex vivo studies have shown that there is indeed thermal heterogeneity in human carotid atherosclerotic plaques (Casscells W, Hawthorn B, David M, Krabach T, Vaughn W K, McAllister H A, Beaman G, Willerson J T. “Thermal detection of cellular infiltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis. Lancet”. 1996,347:1447-1449)
Casscells et al postulate that plaque rupture may be predicted by the heat released by activated macrophages which they suggest are either on the plaque surface or under a thin cap. They postulate that measurement of plaque temperature in vivo could be used to identify plaque at increased risk of rupture In particular they note that 37% of the plaques tested by them had “substantially warmer” regions Such regions are described as being 0.4 to 2.2° C. warmer
This work is discussed further in U.S. Pat. No. 5,935,075, which again discusses the tact that 37% of the plaques had 1 to 5 substantially warmer (0.4 to 2.2° C.) regions per plaque. It is specifically postulated that the temperatures of plaques which are in danger of rupturing will vary from those less at risk by at least 1.5° C.
The work of Casscells et al was carried out on samples of carotid arteries taken at endarterectomy, in the living state but nevertheless not in the subjects. Measurements in the Casscells et al Lancet paper were carried out using a thermistor (Cole-Parmer model 8402-20) with a 24-gauge needle tip and in addition with a Jet Propulsion Laboratory platinum silicide camera. In U.S. Pat. No. 5,935,075 measurements were made by infrared-sensing, in particular with the use of catheters. The methods used comprise placing an optical fibre capable of transmitting radiation proximate to the position at which temperature is to be determined. A balloon encasing a distal end of the fibre is inflated within the blood vessel to cause the balloon to limit flow of fluids within the vessel. Thermal radiation from the vessel is transmitted along the fibre to a detector Clearly, this method necessarily involves limiting flow of fluids within the blood vessel.
Stefanadis et al, in “Thermal Heterogeneity Within Human Atherosclerotic Coronary Arteries Detected in vivo”, Circulation 1999,99,1965-1971, measured various temperatures of human coronary arteries in vivo.
Stefanadis et al determined the difference between temperatures in a control (background) region and temperatures at the surface of a region of interest (ROI). This work concluded that differences between ROI temperatures and background temperatures ranged from 1.55° C. in unstable angina patients to 2.60° C. in acute myocardial infarction patients. Mean differences between ROI and background temperatures were 0.683 in unstable angina patients and 1.472 in acute myocardial infarction patients. Mean values of these differences in stable angina patients were lower, in particular around 0.16° C., but this condition was not believed to be associated with the presence of vulnerable plaque. Indeed, there was no suggestion in this paper that any temperature differences were associated with vulnerable inflamed plaque.
This work was carried out using a thermography catheter The patients tested were those with severe lesions, in particular lesions more than 50% stenosed. This, combined with the particular catheter design used, had the effect that the catheter had to be wedged inside the lesions, severely restricting blood flow through the vessels. We believe that this severe restriction of blood flow led to artificially high temperature measurements